alpha-2-Adrenergic activation of proopiomelanocortin-containing neurons in the arcuate nucleus causes opioid-mediated hypotension and bradycardia.

Treatment of rats for 4 days with alpha-methyldopa, 200 mg/kg/day i.p., increases steady state levels of proopiomelanocortin (POMC) mRNA in the mediobasal hypothalamus, as measured by DNA excess solution hybridization.

Endogenous gamma-aminobutyric acid (GABA) mediates ethanol inhibition of vagally mediated reflex bradycardia elicited from aortic baroreceptors.

We have previously demonstrated that ethanol depresses baroreflex bradycardia by potentiating the similar action of endogenous gamma-aminobutyric acid (GABA) in the medullary dorsal vagal complex. In the present study we examined the relative contribution of the sympathetic vs. the parasympathetic nervous system and aortic vs.

Attenuation of baroreflex changes in cardiac sympathetic efferent activities during acute myocardial ischemia.

Sympathetic efferent activities to the heart during blood pressure changes were investigated in 11 dogs with acute myocardial ischemia. Normalized sympathetic efferent activities recorded in thoracic cardiac nerves decreased or increased as anticipated in response to transient changes in mean arterial pressure (15 to 25 mm Hg with nitroglycerin or phenylephrine, 2 to 8 micrograms/kg, intravenously). A branch of the left circumflex coronary artery was occluded, and the arterial pressure challenges were repeated at 5, 15, and 25 minutes after the occlusion.

A novel acetylcholine receptor-related peptide blocks canine cardiac ganglia and inhibits the nicotinic receptor of PC-12 cells.

A 13 amino acid peptide from the calf muscle acetylcholine receptor has been previously shown to bind both snake neurotoxins and acetylcholine. In the experiments reported here a modified complementary peptide (cAChR) derived from that acetylcholine receptor peptide was tested for biological activity in a canine heart preparation. It was expected that the modified complementary peptide would exhibit either acetylcholine-like effects or acetylcholine inhibiting effects, since, as a complementary peptide to the receptor, it should resemble acetylcholine.

Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms.

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion.